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NA Lachant, A Tomoda and KR Tanaka
Recent investigations have disclosed a decrease in pentose phosphate shunt
activity in hereditary pyrimidine 5'-nucleotidase deficiency. Clinical lead
poisoning is associated with an acquired decrease in pyrimidine
5'-nucleotidase activity. The current investigations were undertaken (1) to
determine if pentose shunt activity was decreased in erythrocytes exposed
to lead, and (2) to compare the mechanism of inhibition to that seen in
hereditary pyrimidine 5'-nucleotidase deficiency. Normal erythrocytes
incubated with lead acetate in vitro demonstrated increased Heinz body
formation, decreased reduced glutathione, a positive ascorbate cyanide
test, and a reversible suppression of pentose shunt activity in the intact
erythrocyte. Lead acetate added to normal red cell hemolysates markedly
inhibited the activities of glucose-6-phosphate dehydrogenase (G6PD) and
phosphofructokinase. The mean Kis of lead for glucose-6-phosphate and
nicotinamide adenine dinucleotide phosphate (NADP) for G6PD were 1.5 microM
and 2.1 microM, respectively, which is within the range of
intraerythrocytic lead concentrations found in clinical lead poisoning.
Magnesium enhanced the ability of lead to inhibit G6PD. Thus, the shortened
erythrocyte survival in lead poisoning appears to be due, in part, to
increased oxidant sensitivity secondary to inhibition of G6PD and the
pentose shunt. The mechanism of shunt inhibition is, in part, similar to
that seen in hereditary pyrimidine 5'-nucleotidase deficiency.
This article has been cited by other articles:
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| Copyright © 1984 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||
